Molecular and Metabolic Evidence for Mitochondrial Defects Associated With β-Cell Dysfunction in a Mouse Model of Type 2 Diabetes

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FIG. 5.
FIG. 5.

Mitochondrial genes/protein changes in islets from 10-week-old mice. A: An integrated genomics and proteomics approach revealed 55 mitochondrial genes (Mito. gene) and 36 mitochondrial proteins (Mito. protein) that were significantly differentially expressed in 10-week-old MKR diabetic islets, 10 of which were changed at both the protein and mRNA level. B: A pictorial comparison of changed mitochondrial protein ratios (Pfold) detected by iTRAQ and microarray (MA) (Gfold) analysis together with functional cluster analysis. Hierarchical clustering was performed using the GoMiner program (27) based on the biological process category in the Gene Ontology Consortium. Colors represent average gene/protein expression changes (MKR/WT) relative to the median (26) with red and green representing an increase or decrease in fold expression, respectively. Red labels: mitochondrial inner membrane. C–F: Differentially expressed mitochondrial genes/proteins in MKR diabetic islets related to the TCA cycle (C), glutamate metabolism (D), fatty acid metabolism (E), and electron transport chains (F). Categorical analysis is based on KEGG pathway database using the GeneMAPP program (28). Data are means ± SE. All changes are significant (P < 0.05) compared with age-matched WT.

This Article

  1. Diabetes vol. 59 no. 2 448-459